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- W4313365989 abstract "Abstract Regulatory T (Treg) cells are indispensable for the maintenance of immune tolerance and the prevention of autoimmunity; however, how Treg cells retain their homeostasis with immune suppressive function remains largely unclear. Here we report that deubiquitinase CYLD plays a critical role in the maintenance of Treg cells. Foxp3− specific CYLD knockout mice showed severe pulmonary inflammation due to preferential migration of Treg cells into the lung and increased interleukin-4 (IL-4) production compared to control mice, which was reversed by the deletion of IL-4. Genome-wide microarray analysis unveiled that Scinderin, a member of the actin-binding gelsolin family, was highly upregulated in CYLD-deficient Treg cells, which contributed to IL-4 production through complex formation with MEK/ERK. Increased IL-4 production by CYLD-deficient Treg cells was significantly rectified by Scinderin ablation. Our findings indicate that CYLD is essential to maintain Treg cell function through regulating Scinderin expression." @default.
- W4313365989 created "2023-01-06" @default.
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- W4313365989 date "2019-05-01" @default.
- W4313365989 modified "2023-09-26" @default.
- W4313365989 title "Deubiquitinase CYLD controls the plasticity of Treg cells by regulation of Scinderin expression" @default.
- W4313365989 doi "https://doi.org/10.4049/jimmunol.202.supp.57.6" @default.
- W4313365989 hasPublicationYear "2019" @default.
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